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Study · In vitro (cells) · 2010

4 results

Melanocortin-4 receptor activation promotes insulin-stimulated mTOR signaling.

Chai B, Li JY, Zhang W, Wu X, Zhang C, Mulholland MW

Peptides31 Jul 2010Cited by 8 (Europe PMC)

PMID20603172 (opens in a new tab)PMCIDPMC3282553 (opens in a new tab)DOI10.1016/j.peptides.2010.06.028 (opens in a new tab)PepBankPUB-20603172
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study4

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In GT1-1 cells expressing MC4R, NDP-MSH dose-dependently enhanced insulin-stimulated mTOR phosphorylation.

    In plain wordsIn cells, NDP-MSH boosted insulin-driven mTOR signalling, and a higher dose gave a bigger boost.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    IncreaseInsulin-stimulated mTOR phosphorylation
    Study

    n: not reported in source

    GT1-1 cell line expressing MC4R
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NDP-MSH dose-dependently enhanced insulin-stimulated mTOR phosphorylation.
    1 context sentence
    Summary · context
    The GT1-1 cell line which expresses MC4R expression was utilized. mTOR signaling was measured by Western blotting analysis using Phospho-mTOR (Ser2448) antibody.
  2. 02LabIn vitro (cells)Mechanism

    In GT1-1 cells, the protein kinase A - cyclic AMP pathway and the MAP kinase pathway were not involved in NDP-MSH actions on insulin-stimulated mTOR phosphorylation.

    In plain wordsIn cells, the PKA-cAMP and MAP kinase pathways did not take part in how NDP-MSH boosted insulin-driven mTOR signalling.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    Not applicableRole of PKA-cAMP and MAP kinase pathways in NDP-MSH enhancement of mTOR phosphorylation
    Study

    n: not reported in source

    GT1-1 cell line expressing MC4R
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The protein kinase A - cyclic AMP pathway and the MAP kinase pathway were not involved in NDP-MSH actions on insulin-stimulated mTOR phosphorylation.
    1 context sentence
    Summary · context
    The GT1-1 cell line which expresses MC4R expression was utilized. mTOR signaling was measured by Western blotting analysis using Phospho-mTOR (Ser2448) antibody.

Studies that did not test the peptide alone2

In this study, Melanotan I (afamelanotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Melanotan I (afamelanotide).

  1. 03LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In GT1-1 cells, the MC4R antagonist SHU9119 blocked the NDP-MSH enhancement of insulin-stimulated mTOR phosphorylation.

    In plain wordsIn cells, an MC4R blocker stopped NDP-MSH from boosting insulin-driven mTOR signalling.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseEffect of MC4R antagonist SHU9119 on NDP-MSH enhancement of mTOR phosphorylation
    Study

    n: not reported in source

    GT1-1 cell line expressing MC4R
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    The MC4R antagonist SHU9119 blocked this effect, demonstrating specificity.
    1 context sentence
    Summary · context
    The GT1-1 cell line which expresses MC4R expression was utilized. mTOR signaling was measured by Western blotting analysis using Phospho-mTOR (Ser2448) antibody.

    In this study, Melanotan I (afamelanotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Melanotan I (afamelanotide).

  2. 04LabNot a test of Melanotan I (afamelanotide) aloneIn vitro (cells)Mechanism

    In GT1-1 cells, the AMP-activated protein kinase agonist AICAR attenuated the NDP-MSH enhancement of insulin-stimulated mTOR phosphorylation.

    In plain wordsIn cells, the AMPK activator AICAR weakened the boost that NDP-MSH gave to insulin-driven mTOR signalling.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseEffect of AMPK agonist AICAR on NDP-MSH enhancement of mTOR phosphorylation
    Study

    n: not reported in source

    GT1-1 cell line expressing MC4R
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    In contrast, the AMP-activated protein kinase agonist, AICAR, attenuated this effect.
    1 context sentence
    Summary · context
    The GT1-1 cell line which expresses MC4R expression was utilized. mTOR signaling was measured by Western blotting analysis using Phospho-mTOR (Ser2448) antibody.

    In this study, Melanotan I (afamelanotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Melanotan I (afamelanotide).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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